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16 results on '"Trovik, Jone"'

2. Mendelian randomization analyses suggest a role for cholesterol in the development of endometrial cancer

Author

Kho, Pik‐Fang, primary, Amant, Frederic, additional, Annibali, Daniela, additional, Ashton, Katie, additional, Attia, John, additional, Auer, Paul L., additional, Beckmann, Matthias W., additional, Black, Amanda, additional, Brinton, Louise, additional, Buchanan, Daniel D., additional, Chanock, Stephen J., additional, Chen, Chu, additional, Chen, Maxine M., additional, Cheng, Timothy H. T., additional, Cook, Linda S., additional, Crous‐Bous, Marta, additional, Czene, Kamila, additional, De Vivo, Immaculata, additional, Dennis, Joe, additional, Dörk, Thilo, additional, Dowdy, Sean C., additional, Dunning, Alison M., additional, Dürst, Matthias, additional, Easton, Douglas F., additional, Ekici, Arif B., additional, Fasching, Peter A., additional, Fridley, Brooke L., additional, Friedenreich, Christine M., additional, García‐Closas, Montserrat, additional, Gaudet, Mia M., additional, Giles, Graham G., additional, Goode, Ellen L., additional, Gorman, Maggie, additional, Haiman, Christopher A., additional, Hall, Per, additional, Hankinson, Susan E., additional, Hein, Alexander, additional, Hillemanns, Peter, additional, Hodgson, Shirley, additional, Hoivik, Erling A., additional, Holliday, Elizabeth G., additional, Hunter, David J., additional, Jones, Angela, additional, Kraft, Peter, additional, Krakstad, Camilla, additional, Lambrechts, Diether, additional, Le Marchand, Loic, additional, Liang, Xiaolin, additional, Lindblom, Annika, additional, Lissowska, Jolanta, additional, Long, Jirong, additional, Lu, Lingeng, additional, Magliocco, Anthony M., additional, Martin, Lynn, additional, McEvoy, Mark, additional, Milne, Roger L., additional, Mints, Miriam, additional, Nassir, Rami, additional, Otton, Geoffrey, additional, Palles, Claire, additional, Pooler, Loreall, additional, Proietto, Tony, additional, Rebbeck, Timothy R., additional, Renner, Stefan P., additional, Risch, Harvey A., additional, Rübner, Matthias, additional, Runnebaum, Ingo, additional, Sacerdote, Carlotta, additional, Sarto, Gloria E., additional, Schumacher, Fredrick, additional, Scott, Rodney J., additional, Setiawan, V. Wendy, additional, Shah, Mitul, additional, Sheng, Xin, additional, Shu, Xiao‐Ou, additional, Southey, Melissa C., additional, Tham, Emma, additional, Tomlinson, Ian, additional, Trovik, Jone, additional, Turman, Constance, additional, Tyrer, Jonathan P., additional, Van Den Berg, David, additional, Wang, Zhaoming, additional, Wentzensen, Nicolas, additional, Xia, Lucy, additional, Xiang, Yong‐Bing, additional, Yang, Hannah P., additional, Yu, Herbert, additional, Zheng, Wei, additional, Webb, Penelope M., additional, Thompson, Deborah J., additional, Spurdle, Amanda B., additional, Glubb, Dylan M., additional, and O'Mara, Tracy A., additional

Published
2020
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4. Preoperative tumor texture analysis on MRI predicts high‐risk disease and reduced survival in endometrial cancer

Author

Ytre‐Hauge, Sigmund, primary, Dybvik, Julie A., additional, Lundervold, Arvid, additional, Salvesen, Øyvind O., additional, Krakstad, Camilla, additional, Fasmer, Kristine E., additional, Werner, Henrica M., additional, Ganeshan, Balaji, additional, Høivik, Erling, additional, Bjørge, Line, additional, Trovik, Jone, additional, and Haldorsen, Ingfrid S., additional

Published
2018
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5. Genetic overlap between endometriosis and endometrial cancer: evidence from cross‐disease genetic correlation and GWAS meta‐analyses

Author

Painter, Jodie N., primary, O'Mara, Tracy A., additional, Morris, Andrew P., additional, Cheng, Timothy H. T., additional, Gorman, Maggie, additional, Martin, Lynn, additional, Hodson, Shirley, additional, Jones, Angela, additional, Martin, Nicholas G., additional, Gordon, Scott, additional, Henders, Anjali K., additional, Attia, John, additional, McEvoy, Mark, additional, Holliday, Elizabeth G., additional, Scott, Rodney J., additional, Webb, Penelope M., additional, Fasching, Peter A., additional, Beckmann, Matthias W., additional, Ekici, Arif B., additional, Hein, Alexander, additional, Rübner, Matthias, additional, Hall, Per, additional, Czene, Kamila, additional, Dörk, Thilo, additional, Dürst, Matthias, additional, Hillemanns, Peter, additional, Runnebaum, Ingo, additional, Lambrechts, Diether, additional, Amant, Frederic, additional, Annibali, Daniela, additional, Depreeuw, Jeroen, additional, Vanderstichele, Adriaan, additional, Goode, Ellen L., additional, Cunningham, Julie M., additional, Dowdy, Sean C., additional, Winham, Stacey J., additional, Trovik, Jone, additional, Hoivik, Erling, additional, Werner, Henrica M. J., additional, Krakstad, Camilla, additional, Ashton, Katie, additional, Otton, Geoffrey, additional, Proietto, Tony, additional, Tham, Emma, additional, Mints, Miriam, additional, Ahmed, Shahana, additional, Healey, Catherine S., additional, Shah, Mitul, additional, Pharoah, Paul D. P., additional, Dunning, Alison M., additional, Dennis, Joe, additional, Bolla, Manjeet K., additional, Michailidou, Kyriaki, additional, Wang, Qin, additional, Tyrer, Jonathan P., additional, Hopper, John L., additional, Peto, Julian, additional, Swerdlow, Anthony J., additional, Burwinkel, Barbara, additional, Brenner, Hermann, additional, Meindl, Alfons, additional, Brauch, Hiltrud, additional, Lindblom, Annika, additional, Chang‐Claude, Jenny, additional, Couch, Fergus J., additional, Giles, Graham G., additional, Kristensen, Vessela N., additional, Cox, Angela, additional, Zondervan, Krina T., additional, Nyholt, Dale R., additional, MacGregor, Stuart, additional, Montgomery, Grant W., additional, Tomlinson, Ian, additional, Easton, Douglas F., additional, Thompson, Deborah J., additional, and Spurdle, Amanda B., additional

Published
2018
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7. Type of vascular invasion in association with progress of endometrial cancer

Author

Visser, Nicole C.M., primary, Werner, Henrica M.J., additional, Krakstad, Camilla, additional, Mauland, Karen K., additional, Trovik, Jone, additional, Massuger, Leon F.A.G., additional, Nagtegaal, Iris D., additional, Pijnenborg, Johanna M.A., additional, Salvesen, Helga B., additional, Bulten, Johan, additional, and Stefansson, Ingunn M., additional

Published
2017
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10. Molecular determinants of outcome with mammalian target of rapamycin inhibition in endometrial cancer

Author

Mackay, Helen J., primary, Eisenhauer, Elizabeth A., additional, Kamel‐Reid, Suzanne, additional, Tsao, Ming, additional, Clarke, Blaise, additional, Karakasis, Katherine, additional, Werner, Henrica M. J., additional, Trovik, Jone, additional, Akslen, Lars A., additional, Salvesen, Helga B., additional, Tu, Dongsheng, additional, and Oza, Amit M., additional

Published
2013
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14. Mendelian randomization analyses suggest a role for cholesterol in the development of endometrial cancer

Author

Kho, Pik-Fang, Amant, Frederic, Annibali, Daniela, Ashton, Katie, Attia, John, Auer, Paul L, Beckmann, Matthias W, Black, Amanda, Brinton, Louise, Buchanan, Daniel D, Chanock, Stephen J, Chen, Chu, Chen, Maxine M, Cheng, Timothy HT, Cook, Linda S, Crous-Bous, Marta, Czene, Kamila, De Vivo, Immaculata, Dennis, Joe, Dörk, Thilo, Dowdy, Sean C, Dunning, Alison M, Dürst, Matthias, Easton, Douglas F, Ekici, Arif B, Fasching, Peter A, Fridley, Brooke L, Friedenreich, Christine M, García-Closas, Montserrat, Gaudet, Mia M, Giles, Graham G, Goode, Ellen L, Gorman, Maggie, Haiman, Christopher A, Hall, Per, Hankinson, Susan E, Hein, Alexander, Hillemanns, Peter, Hodgson, Shirley, Hoivik, Erling A, Holliday, Elizabeth G, Hunter, David J, Jones, Angela, Kraft, Peter, Krakstad, Camilla, Lambrechts, Diether, Le Marchand, Loic, Liang, Xiaolin, Lindblom, Annika, Lissowska, Jolanta, Long, Jirong, Lu, Lingeng, Magliocco, Anthony M, Martin, Lynn, McEvoy, Mark, Milne, Roger L, Mints, Miriam, Nassir, Rami, Otton, Geoffrey, Palles, Claire, Pooler, Loreall, Proietto, Tony, Rebbeck, Timothy R, Renner, Stefan P, Risch, Harvey A, Rübner, Matthias, Runnebaum, Ingo, Sacerdote, Carlotta, Sarto, Gloria E, Schumacher, Fredrick, Scott, Rodney J, Setiawan, V Wendy, Shah, Mitul, Sheng, Xin, Shu, Xiao-Ou, Southey, Melissa C, Tham, Emma, Tomlinson, Ian, Trovik, Jone, Turman, Constance, Tyrer, Jonathan P, Van Den Berg, David, Wang, Zhaoming, Wentzensen, Nicolas, Xia, Lucy, Xiang, Yong-Bing, Yang, Hannah P, Yu, Herbert, Zheng, Wei, Webb, Penelope M, Thompson, Deborah J, Spurdle, Amanda B, Glubb, Dylan M, and O'Mara, Tracy A

Subjects
2. Zero hunger, Risk, Cholesterol, HDL, endometrial cancer risk, Cholesterol, LDL, Mendelian Randomization Analysis, 3. Good health, Endometrial Neoplasms, HDL cholesterol, Case-Control Studies, LDL cholesterol, Mendelian randomization, Humans, lipids (amino acids, peptides, and proteins), Female, triglycerides, Genome-Wide Association Study
Abstract

Blood lipids have been associated with the development of a range of cancers, including breast, lung and colorectal cancer. For endometrial cancer, observational studies have reported inconsistent associations between blood lipids and cancer risk. To reduce biases from unmeasured confounding, we performed a bidirectional, two-sample Mendelian randomization analysis to investigate the relationship between levels of three blood lipids (low-density lipoprotein [LDL] and high-density lipoprotein [HDL] cholesterol, and triglycerides) and endometrial cancer risk. Genetic variants associated with each of these blood lipid levels (P < 5 × 10-8 ) were identified as instrumental variables, and assessed using genome-wide association study data from the Endometrial Cancer Association Consortium (12 906 cases and 108 979 controls) and the Global Lipids Genetic Consortium (n = 188 578). Mendelian randomization analyses found genetically raised LDL cholesterol levels to be associated with lower risks of endometrial cancer of all histologies combined, and of endometrioid and non-endometrioid subtypes. Conversely, higher genetically predicted HDL cholesterol levels were associated with increased risk of non-endometrioid endometrial cancer. After accounting for the potential confounding role of obesity (as measured by genetic variants associated with body mass index), the association between genetically predicted increased LDL cholesterol levels and lower endometrial cancer risk remained significant, especially for non-endometrioid endometrial cancer. There was no evidence to support a role for triglycerides in endometrial cancer development. Our study supports a role for LDL and HDL cholesterol in the development of non-endometrioid endometrial cancer. Further studies are required to understand the mechanisms underlying these findings.

15. Genetic overlap between endometriosis and endometrial cancer: evidence from cross-disease genetic correlation and GWAS meta-analyses

Author

Painter, Jodie N, O'Mara, Tracy A, Morris, Andrew P, Cheng, Timothy HT, Gorman, Maggie, Martin, Lynn, Hodson, Shirley, Jones, Angela, Martin, Nicholas G, Gordon, Scott, Henders, Anjali K, Attia, John, McEvoy, Mark, Holliday, Elizabeth G, Scott, Rodney J, Webb, Penelope M, Fasching, Peter A, Beckmann, Matthias W, Ekici, Arif B, Hein, Alexander, Rübner, Matthias, Hall, Per, Czene, Kamila, Dörk, Thilo, Dürst, Matthias, Hillemanns, Peter, Runnebaum, Ingo, Lambrechts, Diether, Amant, Frederic, Annibali, Daniela, Depreeuw, Jeroen, Vanderstichele, Adriaan, Goode, Ellen L, Cunningham, Julie M, Dowdy, Sean C, Winham, Stacey J, Trovik, Jone, Hoivik, Erling, Werner, Henrica MJ, Krakstad, Camilla, Ashton, Katie, Otton, Geoffrey, Proietto, Tony, Tham, Emma, Mints, Miriam, Ahmed, Shahana, Healey, Catherine S, Shah, Mitul, Pharoah, Paul DP, Dunning, Alison M, Dennis, Joe, Bolla, Manjeet K, Michailidou, Kyriaki, Wang, Qin, Tyrer, Jonathan P, Hopper, John L, Peto, Julian, Swerdlow, Anthony J, Burwinkel, Barbara, Brenner, Hermann, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Chang-Claude, Jenny, Couch, Fergus J, Giles, Graham G, Kristensen, Vessela N, Cox, Angela, Zondervan, Krina T, Nyholt, Dale R, MacGregor, Stuart, Montgomery, Grant W, Tomlinson, Ian, Easton, Douglas F, Thompson, Deborah J, and Spurdle, Amanda B

Subjects
endometriosis, STAT3 Transcription Factor, genome-wide association study, Australia, Receptor-Like Protein Tyrosine Phosphatases, Class 2, Cross-disease analysis, genetic correlation, Polymorphism, Single Nucleotide, 3. Good health, Endometrial Neoplasms, Endometrium, endometrial cancer, Humans, Female, Genetic Predisposition to Disease
Abstract

Epidemiological, biological, and molecular data suggest links between endometriosis and endometrial cancer, with recent epidemiological studies providing evidence for an association between a previous diagnosis of endometriosis and risk of endometrial cancer. We used genetic data as an alternative approach to investigate shared biological etiology of these two diseases. Genetic correlation analysis of summary level statistics from genomewide association studies (GWAS) using LD Score regression revealed moderate but significant genetic correlation (rg = 0.23, P = 9.3 × 10-3 ), and SNP effect concordance analysis provided evidence for significant SNP pleiotropy (P = 6.0 × 10-3 ) and concordance in effect direction (P = 2.0 × 10-3 ) between the two diseases. Cross-disease GWAS meta-analysis highlighted 13 distinct loci associated at P ≤ 10-5 with both endometriosis and endometrial cancer, with one locus (SNP rs2475335) located within PTPRD associated at a genomewide significant level (P = 4.9 × 10-8 , OR = 1.11, 95% CI = 1.07-1.15). PTPRD acts in the STAT3 pathway, which has been implicated in both endometriosis and endometrial cancer. This study demonstrates the value of cross-disease genetic analysis to support epidemiological observations and to identify biological pathways of relevance to multiple diseases.

16. Molecular determinants of outcome with mammalian target of rapamycin inhibition in endometrial cancer.

Author

Mackay HJ, Eisenhauer EA, Kamel-Reid S, Tsao M, Clarke B, Karakasis K, Werner HM, Trovik J, Akslen LA, Salvesen HB, Tu D, and Oza AM

Subjects
Adult, Aged, Aged, 80 and over, Animals, Class I Phosphatidylinositol 3-Kinases, Endometrial Neoplasms genetics, Endometrial Neoplasms pathology, Female, Humans, Middle Aged, Mutation, PTEN Phosphohydrolase genetics, PTEN Phosphohydrolase metabolism, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt metabolism, Signal Transduction drug effects, Sirolimus administration & dosage, Sirolimus analogs & derivatives, TOR Serine-Threonine Kinases antagonists & inhibitors, Endometrial Neoplasms drug therapy, Phosphatidylinositol 3-Kinases genetics, Proto-Oncogene Proteins c-akt genetics, TOR Serine-Threonine Kinases genetics
Abstract

Background: Targeting the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway is of increasing interest as a therapeutic strategy in many tumors. The aim of this study was to identify molecular markers associated with mTOR inhibitor activity in women with metastatic endometrial cancer., Methods: Archival tumor samples were collected from 94 women with recurrent or metastatic endometrial cancer who participated in 3 National Cancer Insitute of Canada Clinical Trials Group phase 2 trials investigating single-agent mTOR inhibitors: IND160A and IND160B (temsirolimus) and IND192 (ridaforolimus). Analyses included mutational profiling using the OncoCarta Panel version 1.0 and immunohistochemical expression of the tumor suppressor gene PTEN (phosphatase and tensin homologue) and stathmin, a marker of PI3K activation. Associations between biomarker results and clinical outcomes were assessed., Results: Mutations were found in 32 of 73 analyzed tumors, PIK3CA (21 patients) was the most common mutated gene. Co-mutations were seen in 8 tumors, most frequently KRAS and PIK3CA (4 cases). PTEN loss was observed in 46 of 85 samples analyzed and increased stathmin expression was observed in 15 of 65 analyzed samples. No correlation was observed between biomarkers and response or progression. In patients taking concurrent metformin, there was a trend toward lower progression, of 11.8% versus 32.5% (P = .14)., Conclusions: No predictive biomarker or combination of biomarkers for mTOR inhibitor activity were identified in this study. Restriction and enrichment of study entry, especially based on archival tumor tissue, should be undertaken with caution in trials using these agents., (© 2013 American Cancer Society.)

Published
2014
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